Method providing atrial anti-tachyarrhythmia therapy

ABSTRACT

The device provides anti-tachyarrhythmia therapy, such as a countershock, to an atrium needing treatment, but delays its delivery for a programmable period of time following an indication of susceptibility to ventricular tachyarrhythmia (VT). This reduces the risk of reinducing VT during a period in which the heart is abnormally metabolically vulnerable to VT, including ventricular fibrillation (VF). The delay time may be independently programmed for different indications of VT, and may be synchronized to and delayed from the R-wave. The delay time may be adjusted, such as to exceed one second, or even to exceed several hours, in order to accommodate the metabolic abnormal susceptibility of the particular patient in the wide range of patients needing treatment of atrial tachyarrhythmias.

This application claims the benefit under 35 U.S.C. §119(e) of U.S.Provisional Application No. 60/055,181, filed on Aug. 8, 1997, which isincorporated herein by reference.

TECHNICAL FIELD OF THE INVENTION

This invention relates generally to cardiac rhythm management devicesand methods, and more particularly to an implantable device, such as acardioverter-defibrillator, and method for treating atrialtachyarrhythmias.

BACKGROUND OF THE INVENTION

Atrial tachyarrhythmias are quite common, and are seen even in patientswho are not acutely ill. One such atrial tachyarrhythmia, atrialfibrillation, does not usually pose an immediate threat to the patient'slife, but prolonged atrial fibrillation can compromise patienthemodynamics. Inadequate blood flow due to atrial fibrillation may leadto blood clots, which increase the risk of strokes. Other symptoms mayinclude palpitations of the heart, dizziness, or loss of consciousness.

One method of treating atrial fibrillation is to deliver a countershockto terminate the arrhythmia. For example, the countershock may beapplied via an external or implantable defibrillator. However, thismethod of treating atrial fibrillation risks causing ventriculartachyarrhythmias, including life-threatening ventricular fibrillation.

One method of reducing the risk of ventricular fibrillation is bysynchronizing the delivery of a countershock to an electricalventricular activation (R-wave) of the heart. There is, however, a needin the art to further reduce the risk of inducing ventriculartachyarrhythmias, such as life-threatening ventricular fibrillation,during the countershock treatment of comparatively less exigent atrialtachyarrhythmias.

SUMMARY OF THE INVENTION

The present invention provides a method of applying anti-tachyarrhythmiatherapy, such as a countershock, to the heart. From the atrium of theheart, atrial activity needing anti-tachyarrhythmia therapy is detected.Ventricular activity is monitored for an indication of abnormalsusceptibility to ventricular tachyarrhythmia. Anti-tachyarrhythmiatherapy is delivered to the atrium in response to the detected atrialtachyarrhythmia activity. But the atrial tachyarrhythmia therapy isdelayed for a first time delay if the indication of abnormalsusceptibility to ventricular tachyarrhythmia is detected.

The present invention also provides an device, such as an implantablecardioverter-defibrillator, for delivering anti-tachyarrhythmia therapyto the heart. An atrial receiver receives an atrial heart activitysignal from an atrium of the heart. A ventricular receiver receives aventricular heart activity signal from the ventricle of the heart. Acontroller controls the delivery of the anti-tachyarrhythmia therapy tothe atrium in response to the atrial heart activity signal indicating aneed for the anti-tachyarrhythmia therapy. The controller includes afirst timer for delaying the delivery, by a first time delay, of theanti-tachyarrhythmia therapy to the atrium in response to theventricular heart activity signal indicating abnormal susceptibility toa ventricular tachyarrhythmia.

In one embodiment, the countershock or other anti-tachyarrhythmiatherapy is synchronized to or delayed from the R-wave. In anotherembodiment, following the indication of abnormal susceptibility to aventricular tachyarrhythmia, the first timer is reset and the value ofthe first time delay is adjusted according to the particular type ofindication of abnormal susceptibility to a ventricular tachyarrhythmia.The value of the first time delay can be programmed depending on thepatient's vulnerability to ventricular tachyarrhythmia The delay can beprogrammed to exceed approximately one second or approximately severalhours. In one embodiment, the first timer is reset and the value of thefirst time delay is adjusted subsequent to delivery of an atrialcountershock.

The present invention delays delivery of atrial anti-tachyarrhythmiatherapy when an indication of abnormal susceptibility to a ventriculartachyarrhythmia is present. As a result, the present invention reducesthe risk of reinducing ventricular tachyarrhythmias, such aslife-threatening ventricular fibrillation, which can be caused by thedelivery of anti-tachyarrhythmia therapy to the atrium.

BRIEF DESCRIPTION OF THE DRAWINGS

In the drawings, like numerals describe substantially similar componentsthroughout the several views.

FIG. 1 is a flow chart illustrating one embodiment of a method ofdelivering an atrial countershock to treat tachyarrhythmias.

FIG. 2 is a flow chart illustrating an alternate embodiment of themethod illustrated in FIG. 1, in which a first time delay is adjustedaccording to a type of indication of abnormal susceptibility toventricular tachyarrhythmia.

FIG. 3 is a flow chart illustrating an alternate embodiment of themethod illustrated in FIG. 1 that rechecks for atrial tachyarrhythmiaafter waiting until a first time delay expires.

FIG. 4 is a flow chart illustrating an alternate embodiment of themethod illustrated in FIG. 1, in which a first timer is reset afterdelivery of anti-tachyarrhythmia therapy to the atrium.

FIG. 5 is a flow chart illustrating, in more detail, one embodiment ofthe step of delivering the atrial anti-tachyarrhythmia therapy in FIGS.1-4.

FIG. 6 is a schematic diagram illustrating one embodiment of the presentinvention in relation to a heart to which it delivers therapy.

DETAILED DESCRIPTION OF THE INVENTION

In the following detailed description, reference is made to theaccompanying drawings which form a part hereof, and in which is shown byway of illustration specific embodiments in which the invention may bepracticed. These embodiments are described in sufficient detail toenable those skilled in the art to practice the invention, and it is tobe understood that the embodiments may be combined, or that otherembodiments may be utilized and that structural, logical and electricalchanges may be made without departing from the spirit and scope of thepresent invention. The following detailed description is, therefore, notto be taken in a limiting sense, and the scope of the present inventionis defined by the appended claims and their equivalents.

The present invention provides anti-tachyarrhythmia therapy to an atriumof a heart. In this application, atrial tachyarrhythmias (ATs) areunderstood to comprise any atrial tachyarrhythmia including, but notlimited to: sinus tachycardia, atrial flutter, atrial tachycardia,atrial fibrillation, AV nodal reentrant tachycardia. Ventriculartachyarrhythmias (VTs) are understood to comprise any ventriculartachyarrhythmia including, but not limited to, ventricular fibrillation(VF). Cardioversion and defibrillation are understood to refer generallyto any treatment of a cardiac arrhythmia by an electrical countershock.Cardioverter and defibrillator are understood to refer generally to anydevice capable of treating a cardiac arrhythmia through an electricalcountershock. Anti-tachyarrhythmia therapy is understood to comprisetreatment of atrial tachyarrhythmia by electrical countershock,anti-tachyarrhythmia drugs, or anti-tachycardia pacing.

The present invention provides anti-tachyarrhythmia therapy, such ascountershock therapy, to the atrium of the heart such that the risk ofventricular tachyarrhythmias, particularly that of life-threateningventricular fibrillation, is minimized. As described in detail below,the present invention recognizes time periods in which the ventricle ofthe heart may be abnormally susceptible to ventricular tachyarrhythmias,and avoids treatment of atrial tachyarrhythmias during these vulnerableperiods.

FIG. 1 is a flow chart illustrating one embodiment of the methodaccording to the present invention. In FIG. 1, a first timer formeasuring a first time delay is initially reset at step 100. An atriumof the heart and a ventricle of the heart are concurrently andcontinuously monitored at steps 110A-B. The atrium is monitored for anyatrial tachyarrhythmia activity needing anti-tachyarrhythmia therapy,such as atrial fibrillation. The ventricle is monitored for anyventricular vulnerability, i.e. any indication of abnormalsusceptibility to a ventricular tachyarrhythmia (VT), and particularlyfor abnormal susceptibility to ventricular fibrillation (VF). Sensedelectrical indications of abnormal susceptibility to a ventriculartachyarrhythmia may include, but are not limited to: one or morepremature ventricular contractions (PVCs); a particular number ofpremature ventricular contractions detected during a particular thirdperiod of time, such as, for example, 6 to 8 premature ventricularcontractions occurring within an hour; a particular number of successivepremature ventricular contractions; ventricular tachycardia bigeminy;non-sustained monomorphic or polymorphic ventricular tachycardia;sustained monomorphic or polymorphic ventricular tachycardia; and,ventricular fibrillation.

Indications of ventricular abnormal susceptibility are understood toinclude actual instances of ventricular tachyarrhythmia, includingventricular fibrillation, and any other indication of abnormalsusceptibility to ventricular tachyarrhythmia. For example, othersuitable indications of abnormal susceptibility to ventriculartachyarrhythmia may include chemical or other indications. In oneembodiment of the present invention, the actual delivery of atrialanti-tachyarrhythmia therapy, such as a countershock, is itself definedas an indication of abnormal susceptibility to ventriculartachyarrhythmia.

Indications of abnormal susceptibility to ventricular tachyarrhythmiaare understood not to include the T-wave time periods within a cardiaccycle during which the heart is normally particularly vulnerable to anexternal stimulus. However, in one embodiment of the present inventionthat is described below, such normal time periods of vulnerability arealso avoided by the present invention. It is also understood that theindications of abnormal susceptibility to ventricular tachyarrhythmiaare programmably adjustable by the physician. Thus, those indications ofsusceptibility to ventricular tachyarrhythmia that are consideredabnormal may vary from patient to patient.

One aspect of the present invention, is the recognition that suchindications of abnormal susceptibility to ventricular tachyarrhythmiadefine time periods in which the heart is metabolically abnormallysusceptible to induction of ventricular tachyarrhythmias, includinglife-threatening ventricular fibrillation. As described in detail below,the present invention avoids delivering anti-tachyarrhythmia therapy,such as countershock treatment, to the atrium during these vulnerabletime periods.

At step 120, if the ongoing ventricular monitoring of step 110B providesno indication of abnormal susceptibility to ventricular tachyarrhythmia,the ongoing monitoring of the atrium and ventricle continues atconcurrent steps 110A-B. However, if abnormal susceptibility toventricular tachyarrhythmia is indicated at step 120, the first timerfor measuring the first time delay is reset at step 100 before theongoing monitoring of the atrium and ventricle continues at concurrentsteps 110A-B. Thus, the first timer measures the elapsed time from thelast indication of ventricular tachyarrhythmia, if any.

Similarly, at step 140 if the ongoing atrial monitoring of step 110Aprovides no indication of a detected atrial tachyarrhythmia, the ongoingmonitoring of the atrium and ventricle continues at concurrent steps110A-B. When, at step 140, the atrial monitoring indicates detection ofan atrial tachyarrhythmia, the present invention is typically capable ofrecognizing and distinguishing, at step 145, between different forms ofatrial tachyarrhythmia detected at step 140, such thatanti-tachyarrhythmia therapy is only delivered in response to particularforms of atrial tachyarrhythmia, e.g. atrial fibrillation (AF), asdescribed below. If the detected atrial tachyarrhythmia does notindicate, at step 145, that anti-tachyarrhythmia therapy should bedelivered, the monitoring of the atrium and ventricle is continued atconcurrent steps 110A-B.

If, at step 145, the detected atrial tachyarrhythmia indicates thatanti-tachyarrhythmia therapy should be delivered, the first timer formeasuring the first time delay is checked at step 150. If the first timedelay is expired (i.e., if the first timer's measurement of the elapsedtime from the last indication of abnormal susceptibility to ventriculartachyarrhythmia, if any, exceeds the programmably adjustable value ofthe first time delay), a countershock or other anti-tachyarrhythmiatherapy is delivered at step 160 to the atrium in which the atrialtachyarrhythmia was detected.

If, however, the first time delay has not expired (i.e., if the firsttimer's measurement of the elapsed time from the last indication ofabnormal susceptibility to ventricular tachyarrhythmia, if any, does notexceed the programmably adjustable value of the first time delay),anti-tachyarrhythmia therapy is delayed at step 170 until the first timedelay has expired. At step 170, after the first time delay expires, thecountershock or other anti-tachyarrhythmia therapy is delivered to theatrium at step 160. In this embodiment, the ongoing monitoring of theatrium and the ventricle may be optionally blanked during delivery ofthe anti-tachyarrhythmia therapy at step 110, but the ongoing monitoringcontinues following the delivery of the anti-tachyarrhythmia therapy tothe atrium at step 160.

As set forth above, the first time delay is typically programmablyadjusted by the physician to accommodate the individual degree ofmetabolic vulnerability of the patient to ventricular tachyarrhythmia,including ventricular fibrillation. In the diverse patient populationthat is susceptible to atrial tachyarrhythmia, the metabolicvulnerability of the particular patient to ventricular tachyarrhythmia,including ventricular fibrillation, will vary widely. Thus, the durationof the first time delay, which follows the above-described indicationsof abnormal susceptibility to ventricular tachyarrhythmia, will alsovary widely to accommodate this variability in the patient population.

The period of metabolic vulnerability that the first time delay shouldexceed is typically longer than the duration of a cardiac cycle, i.e.time between successive heartbeats. Therefore, the first time delay istypically adjustably programmed to a value exceeding one second. Thefirst time delay may even be programmed to exceed one hour or severalhours for patients that are abnormally metabolically vulnerable toventricular tachyarrhythmia, such as ventricular fibrillation, followingrecent indications of abnormal susceptibility to ventriculartachyarrhythmia.

FIG. 2 is a flow chart illustrating one embodiment of the presentinvention in which the duration of the first time delay depends on theparticular type of one or more recent particular indications of abnormalsusceptibility to ventricular tachyarrhythmia. This embodiment allowsthe physician to independently program different values of the firsttime delay to correspond respectively to different types of indicationsof abnormal susceptibility to ventricular tachyarrhythmia. For example,one indication of abnormal susceptibility to ventricular tachyarrhythmiamay be a single premature ventricular contraction, for which thephysician may program a corresponding first time delay to be severalseconds. Another indication of abnormal susceptibility to ventriculartachyarrhythmia may be an actual episode of ventricular fibrillation,for which the physician may program a corresponding first time delay tobe several hours.

The method illustrated in FIG. 2 closely follows that illustrated anddescribed above with respect to FIG. 1, and like blocks or steps areindicated by the like numbers. However, in FIG. 2 at step 200, theinvention recognizes the type of the most recent indication of abnormalsusceptibility to ventricular tachyarrhythmia, and sets the value of thefirst time delay accordingly, unless doing so would cut short anunexpired longer first time delay corresponding to a previous indicationof abnormal susceptibility to ventricular tachyarrhythmia. The inventionthen resets the first timer at step 100 before continuing the ongoingmonitoring of the atrium and the ventricle at concurrent steps 110A-B.

FIG. 3 is a flow chart illustrating an alternate embodiment of themethod5 according to the present invention. The method illustrated inFIG. 3 closely follows that illustrated and described above with respectto FIG. 1, and like blocks or steps are indicated by the like numbers.However, in FIG. 3, after waiting until the first time delay expires atstep 170, the present invention rechecks whether atrial tachyarrhythmiais detected at step 140. If atrial tachyarrhythmia is not present atstep 140, or is determined at step 145 to be of a type not requiringtreatment, the ongoing monitoring of the atrium and the ventricle isresumed at concurrent steps 110A-B. If atrial tachyarrhythmia is stillpresent at step 140, and is determined at step 145 to be of a typerequiring treatment, the invention finds the first time delay to beexpired at step 150, and proceeds to deliver anti-tachyarrhythmiatherapy, such as a countershock, to the atrium at step 160.

FIG. 4 is a flow chart illustrating an alternate embodiment of themethod according to the present invention. The method illustrated inFIG. 4 closely follows that illustrated and described above with respectto FIG. 1, and like blocks or steps are indicated by the like numbers.However, in FIG. 4, after the anti-tachyarrhythmia therapy, such as acountershock, is delivered to the atrium at step 160, the timer formeasuring the first time delay is reset at step 100 before the ongoingmonitoring of the atrium and ventricle continues at concurrent steps110A-B. Thus, according to the method illustrated in FIG. 4, subsequentatrial anti-tachyarrhythmia therapy is delayed by at least the firsttime delay regardless of whether or not ventricular tachyarrhythmia isindicated at step 120. By contrast, according to the embodimentillustrated in FIG. 1, subsequent atrial anti-tachyarrhythmia therapycan be delivered immediately, i.e. without waiting for the duration offirst time delay, if ventricular tachyarrhythmia is not indicatedsubsequent to a first delivery of atrial anti-tachyarrhythmia therapy.

In FIGS. 1-4, delivery of the atrial anti-tachyarrhythmia therapy, suchas a countershock, at step 160 typically includes synchronizing thedelivery to ventricular activations (R-waves) of the heart. FIG. 5 is aflow chart illustrating, by way of example, one embodiment of thedetails of step 160 in more detail. The method illustrated in FIG. 5closely follows that illustrated and described above with respect toFIG. 1, and like blocks or steps are indicated by the like numbers.However, the additional details of step 160 that are illustrated in FIG.5 may also be applicable to other embodiments of the present invention,such as those illustrated in FIGS. 1-4.

In FIG. 5, delivery of anti-tachyarrhythmia therapy at step 160 includessynchronizing to one of the ventricular activations (R-waves) of theheart, at step 500. Such ventricular activations are detected during theongoing monitoring of the ventricle at step 110B. Synchronizing thedelivery of the anti-tachyarrhythmia therapy to one of the ventricularactivations reduces the risk of delivering a countershock to the heartduring the T-wave period in a cardiac cycle in which the heart isparticularly vulnerable to induction of ventricular fibrillation. Atstep 510, an optional second time delay is provided to offset in timefrom the R-wave the delivery of the anti-tachyarrhythmia therapy. In oneembodiment, the second time delay is shorter than the approximately 250millisecond interval between the R-wave and the T-wave that immediatelyfollows. The anti-tachyarrhythmia therapy, such as a countershock, isdelivered to the atrium at step 520 after the second time delay hasexpired. In this embodiment, the anti-tachyarrhythmia therapy comprisesa countershock delivered synchronously to and optionally delayed fromthe ventricular activation (R-wave), such that the atrial countershockis delivered between an R-wave and a T-wave.

FIG. 6 is a schematic illustration of one embodiment of an implantabledevice, such as implantable cardioverter-defibrillator 300, fordelivering anti-tachyarrhythmia therapy according to the presentinvention. Cardioverter-defibrillator 300 is illustrated in relation toa heart 305 to which it delivers therapy. Ventricular heart activity issensed by a ventricular sensor such as electrodes 310 and 315, which areindependently electrically coupled through ventricular lead 320 toventricular receiver 325 in cardioverter-defibrillator 300. Atrial heartactivity is sensed by an atrial sensor, such as atrial electrodes 330and 335, which are independently electrically coupled through atriallead 340 to atrial receiver 345 in cardioverter-defibrillator 300.

For the embodiment of the cardioverter-defibrillator 300 illustrated inFIG. 6, the received ventricular and atrial signals may undergo furthersignal processing, including amplification, analog filtering, andanalog-to-digital conversion in respective ventricular and atrial signalprocessing channels 350 and 355 before being provided to a controller360. Controller 360 typically includes a microprocessor and associatedinterface circuitry. Cardioverter-defibrillator 300 also includes: abattery 365, for providing power to its various electrical components;transceiver 370, for communication with external remote transceiver 375;atrial therapy circuit 380, for providing anti-tachyarrhythmia therapy,such as an electrical countershock pulse, to the atrium of the heart305. Atrial lead 340 and atrial electrodes 330 and 335 are alsoelectrically coupled to cardioverter-defibrillator 300 for delivery ofthe anti-tachyarrhythmia therapy from cardioverter-defibrillator 300 tothe atrium of the heart 305.

Controller 360 is capable of detecting and distinguishing between theindications of ventricular tachyarrhythmia, as described above withrespect to FIG. 1. Controller 360 is also capable of detecting theventricular activations (R-waves) of the heart 305, as described abovewith respect to FIG. 5. Controller 360 is also capable of detectingatrial activity and distinguishing between atrial tachyarrhythmiaactivity needing anti-tachyarrhythmia therapy, such as atrialfibrillation, and atrial tachyarrhythmia activity not requiringanti-tachyarrhythmia therapy. Controller 360 also includes a first timer385 for measuring an elapsed time from an indication of abnormalsusceptibility to ventricular tachyarrhythmia. The elapsed time of firsttimer 385 is compared to a first time delay value that is externallyadjustably programmable from remote transceiver 375 through transceiver370.

First timer 385 may be an analog timer or digital counter, or a softwaretimer, or any other suitable timer implementation. The value of thefirst time delay is adjustably programmed by the physician to exceed theestimated time period of metabolic vulnerability for a patient followinga recent indication of abnormal susceptibility to ventriculartachyarrhythmia. First timer 385 is reset at each indication of abnormalsusceptibility to ventricular tachyarrhythmia, and in one embodiment,the first time delay is also adjusted to correspond to a value that isparticularized to each type of indication of ventriculartachyarrhythmia, as described above with respect to FIG. 2.

When controller 360 detects an atrial tachyarrhythmia needing therapy,it provides anti-tachyarrhythmia therapy, such as a countershock,through atrial therapy circuit 380, to the atrium when a sufficient timehas elapsed since the last indication of abnormal susceptibility toventricular tachyarrhythmia (i.e., when first timer 385 indicates thatthe first time delay has expired). If, upon detection of the atrialtachyarrhythmia, the first time delay has not expired, controller 360waits until the first time delay 385 has expired. In one embodiment,controller 360 rechecks whether atrial tachyarrhythmia is still present,after waiting until the first time delay 385 has expired, beforedelivering anti-tachyarrhythmia therapy to the atrium, as describedabove with respect to FIG. 3. In another embodiment, controller 360 isimmediately capable of delivering subsequent atrial anti-tachyarrhythmiatherapy, as described above with respect to FIGS. 1-2. In anotherembodiment, controller 360 resets first timer 385 after atrialanti-tachyarrhythmia therapy is delivered, such that subsequent atrialanti-tachyarrhythmia therapy is inhibited for a corresponding period oftime, as described above with respect to FIG. 4. In one embodiment,delivery of atrial anti-tachyarrhythmia therapy is itself defined as anindication of abnormal susceptibility to ventricular tachyarrhythmiahaving a separate corresponding first time delay value. In thisembodiment, after delivery of atrial anti-tachyarrhythmia therapy,controller 360 adjusts the first time delay accordingly, as describedabove with respect to FIG. 2.

Controller 360 typically also includes synchronizer 390 forsynchronizing delivery of the atrial anti-tachyarrhythmia therapy to aventricular activation (R-wave) sensed by ventricular receiver 325, asdescribed above with respect to FIG. 5. In one embodiment, synchronizer390 includes a second timer for delaying the synchronous delivery of theatrial anti-tachyarrhythmia therapy for a second time delay, asdescribed above with respect to FIG. 5.

Thus, the present invention provides anti-tachyarrhythmia therapy to theatrium of the heart such that the risk of ventricular tachyarrhythmias,particularly that of life-threatening ventricular fibrillation, isminimized. The present invention recognizes that the heart ismetabolically abnormally susceptible to reinduction of ventriculartachyarrhythmias during the time periods that follow indications ofabnormal susceptibility to ventricular tachyarrhythmias. The presentinvention avoids atrial anti-tachyarrhythmia therapy, such ascountershock treatment, during these vulnerable periods, therebyreducing the risk of inducing ventricular fibrillation.

It should be understood that the present invention may be implemented,for example, in a cardioverter-defibrillator that providesanti-tachyarrhythmia therapy, such as a countershock, to the atriumonly. The present invention may also be implemented as part of adual-chamber cardioverter-defibrillator that providesanti-tachyarrhythmia therapy, such as a countershock, to both the atriumand ventricle. Also, the anti-tachyarrhythmia therapy may also includetherapy other than countershocks without departing from the scope andspirit of the present invention. For example, anti-tachycardia pacing ordrug delivery therapy could be similarly delayed from theabove-described indications of ventricular tachyarrhythmias. In anotherexample, bradycardia pacing therapy could be combined with theabove-described functionality of the present invention.

It is to be understood that the above description is intended to beillustrative, and not restrictive. Many other embodiments will beapparent to those of skill in the art upon reviewing the abovedescription. The scope of the invention should, therefore, be determinedwith reference to the appended claims, along with the full scope ofequivalents to which such claims are entitled.

What is claimed is:
 1. A method of applying anti-tachyarrhythmia therapyto a heart, the method including the steps of:detecting, from an atriumof the heart, atrial tachyarrhythmia activity indicative of a need forthe anti-tachyarrhythmia therapy; monitoring ventricular activity of theheart for an indication of abnormal susceptibility to a ventriculartachyarrhythmia; and applying the anti-tachyarrhythmia therapy to theatrium in response to the detected atrial tachyarrhythmia activity, butdelaying the application of the anti-tachyarrhythmia therapy for a firsttime delay if the indication of abnormal susceptibility to theventricular tachyarrhythmia is detected.
 2. The method of claim 1,further comprising the step of detecting ventricular activations of theheart.
 3. The method of claim 2, including synchronizing applying theanti-tachyarrhythmia therapy to one of the detected ventricularactivations of the heart.
 4. The method of claim 3, including delayingapplying the anti-tachyarrhythmia therapy for a second time delay fromthe one of the detected ventricular activations of the heart.
 5. Themethod of claim 4, including detecting T-waves, determining an intervalbetween the one of the detected ventricular activations of the heart anda T-wave immediately following the one of the detected ventricularactivations of the heart, wherein the second time delay is shorter thanthe interval.
 6. The method of claim 1, wherein the first time delayexceeds approximately one second.
 7. The method of claim 1, wherein thefirst time delay exceeds approximately one hour.
 8. The method of claim1, wherein the first time delay exceeds approximately several hours. 9.The method of claim 1, including extending the first time delay past aperiod in which the ventricle is abnormally susceptible totachyarrhythmia resulting from the anti-tachyarrhythmia therapy appliedto the atrium.
 10. The method of claim 1, wherein the first time delayis adjustable.
 11. The method of claim 10, including programming thefirst time delay based upon an abnormal susceptibility of an individualpatient to ventricular tachyarrhythmia in response to theanti-tachyarrhythmia therapy applied to the atrium.
 12. The method ofclaim 1, including setting the first time delay based on the type of theindication of abnormal susceptibility to the ventriculartachyarrhythmia.
 13. The method of claim 1, wherein the first time delayis adjusted subsequent to the step of applying the anti-tachyarrhythmiatherapy to the atrium.
 14. The method of claim 1, wherein the indicationof abnormal susceptibility to the ventricular tachyarrhythmia includesat least one premature ventricular contraction.
 15. The method of claim14, wherein the indication of abnormal susceptibility to the ventriculartachyarrhythmia includes a number of premature ventricular contractionsdetected over a third period of time.
 16. The method of claim 14,wherein the indication of abnormal susceptibility to the ventriculartachyarrhythmia includes a number of successive premature ventricularcontractions.
 17. The method of claim 1, wherein the indication ofabnormal susceptibility to the ventricular tachyarrhythmia includesnon-sustained ventricular tachycardia.
 18. The method of claim 1,wherein the indication of abnormal susceptibility to the ventriculartachyarrhythmia includes ventricular tachycardia.
 19. The method ofclaim 1, wherein the indication of abnormal susceptibility to theventricular tachyarrhythmia includes ventricular fibrillation.
 20. Themethod of claim 1, wherein the indication of abnormal susceptibility tothe ventricular tachyarrhythmia is chemical.
 21. The method of claim 1,wherein the indication of abnormal susceptibility to the ventriculartachyarrhythmia is anti-tachyarrhythmia therapy that was previouslydelivered to the heart.
 22. The method of claim 1, wherein theanti-tachyarrhythmia therapy includes an electrical countershock. 23.The method of claim 1, wherein the anti-tachyarrhythmia therapy includesdelivery of an anti-tachyarrhythmia drug.
 24. The method of claim 1,wherein the anti-tachyarrhythmia therapy includes anti-tachycardiapacing.
 25. A method of applying anti-tachyarrhythmia therapy to aheart, the method including the steps of:detecting, from an atrium ofthe heart, atrial tachyarrhythmia activity indicative of a need for theanti-tachyarrhythmia therapy; determining whether a ventricle of theheart is abnormally susceptible to fibrillation; and applyinganti-tachyarrhythmia therapy to the atrium in response to the detectedatrial tachyarrhythmia activity, but delaying the application of theanti-tachyarrhythmia therapy for at least a time period in which theventricle of the heart is abnormally susceptible to fibrillation.